ReviewActa neuropathologica2020
From the prion-like propagation hypothesis to therapeutic strategies of anti-tau immunotherapy.
Review in Acta neuropathologica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
103 citing papers in PubMed, 1 synthesis or guideline pooled it, 185 citations in OpenAlex.
- The FDA-approved anti-amyloid-β monoclonal antibodies for the treatment of Alzheimer's disease: a systematic review and meta-analysis of randomized controlled trials.European journal of medical research · 2023Pooled it
- ADAMANT: a placebo-controlled randomized phase 2 study of AADvac1, an active immunotherapy against pathological tau in Alzheimer's disease.Nature aging · 2021Trial
- Regional brain metabolism and metabolic connectivity alterations in corticobasal syndrome assessed with [European journal of nuclear medicine and molecular imaging · 2026Article
- "S-Tau-Lled" Lysosomes Disrupt Autophagic Processes in Neurodegeneration.Traffic (Copenhagen, Denmark) · 2026Article
- A third-generation, high-affinity biparatopic anti-tau antibody inhibits intracellular tau aggregation seeded by Alzheimer's brain extracts.Alzheimer's research & therapy · 2026Article
- Cerebral Intramural Cells: A Missing Cellular Link Between Vascular Aging and Alzheimer's Disease.International journal of molecular sciences · 2026Review
- Amplification of seeding-competent tau aggregates by PMCA in human and experimental tauopathies.Acta neuropathologica communications · 2026Article
- Tau-mediated Mechanisms in Alzheimer's Disease Pathogenesis.Molecular neurobiology · 2026Review
- Bridging autophagy and endolysosomal dysfunction: Role of bridging integrator 1 in Alzheimer's disease.Neural regeneration research · 2026Article
- Meningeal lymphatic dysfunction in Alzheimer's disease: molecular mechanisms, clinical implications, and future perspectives.Molecular neurodegeneration · 2026Review
- Rhizomes as Multi-Target Pharmacological Platforms Against Tauopathy: Neuro-Metabolic Crosstalk, Drug-Likeness, and Translational Challenges.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Senescent cells in systemic aging: SASP heterogeneity, immune escape, and endocrine modulation.Biogerontology · 2026Review
- Bridging the gaps in alzheimer's disease: a comprehensive review of current and emerging therapies.Inflammopharmacology · 2026Review
- Exploring Lymphovenous Anastomosis for Alzheimer Disease: Addressing Brain Lymphatic Dysfunction, Feasibility, and Outcome Metrics.Plastic and reconstructive surgery · 2026Review
- Safety, tolerability and biomarker results of bepranemab in participants with progressive supranuclear palsy: a randomised, multicentre, double-blind, placebo-controlled, phase 1b trial.BMJ neurology open · 2026Article
- Stratification of brain-derived extracellular vesicles of Alzheimer's disease patients indicates a unique proteomic content and a higher seeding capacity of small extracellular vesicles.Translational neurodegeneration · 2025Article
- Primary age-related tauopathy.Acta neuropathologica · 2025Review
- Anti-tau VHH therapy against PHF6: a safe approach to slowing the phenotype of tau pathology.Alzheimer's research & therapy · 2025Article
- Biochemical characterization of Tau protein changes and amyloid dynamics in a novel non-transgenic rat model of tauopathy.Journal of neural transmission (Vienna, Austria : 1996) · 2025Article
- Advancements in Proteolysis Targeting Chimeras for Targeted Therapeutic Strategies in Alzheimer's Disease.Molecular neurobiology · 2025Review
43 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 4 countries.
Funding
Abstract
The term "propagon" is used to define proteins that may transmit misfolding in vitro, in tissues or in organisms. Among propagons, misfolded tau is thought to be involved in the pathogenic mechanisms of various "tauopathies" that include Alzheimer's disease, progressive supranuclear palsy, and argyrophilic grain disease. Here, we review the available data in the literature and point out how the prion-like tau propagation has been extended from Alzheimer's disease to tauopathies. First, in Alzheimer's disease, the progression of tau aggregation follows stereotypical anatomical stages which may be considered as spreading. The mechanisms of the propagation are now subject to intensive and controversial research. It has been shown that tau may be secreted in the interstitial fluid in an active manner as reflected by high and constant concentration of extracellular tau during Alzheimer's pathology. Animal and cell models have been devised to mimic tau seeding and propagation, and despite their limitations, they have further supported to the prion-like propagation hypothesis. Finally, such new ways of thinking have led to different therapeutic strategies in anti-tau immunotherapy among tauopathies and have stimulated new clinical trials. However, it appears that the prion-like propagation hypothesis mainly relies on data obtained in Alzheimer's disease. From this review, it appears that further studies are needed (1) to characterize extracellular tau species, (2) to find the right pathological tau species to target, (3) to follow in vivo tau pathology by brain imaging and biomarkers and (4) to interpret current clinical trial results aimed at reducing the progression of these pathologies. Such inputs will be essential to have a comprehensive view of these promising therapeutic strategies in tauopathies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.